Cardiac resynchronization therapy (CRT) is a promising and accepted device therapy for patients with systolic heart failure classified in New York Heart Association (NYHA) class III and IV. Current (2003) indications include patients who, despite optimal medication, are symptomatic, and who demonstrate LV asynchrony. The latter occurs in patients with left bundle branch block (LBBB) and typically presents with a QRS width (measured on an ECG machine) of greater than about 130-150 ms. Herein, “asynchrony” is characterized by a delay in systolic contraction between the intraventricular septum and the left ventricular (LV) free wall.
Currently available CRT bi-ventricular pacing generally employs one lead positioned in operative communication with the right ventricle (RV) and one lead in operative communication with a portion of one of the tributaries of the coronary venous system. The myocardial venous system provides a pathway for deployment of LV stimulation of the lead (and associated electrodes) to operatively communicate with the LV. In most patients, an additional lead is deployed to the right atrium (RA) for atrioventricular (AV) synchronization during pacing. Exceptions for placement of the atrial lead include patients suffering from chronic atrial fibrillation (AF) or having a relatively high AF “burden.” According to such CRT delivery, electrical stimulation of both the RV and LV operates to assist ventricular asynchrony and increase contractility (as measured by ventricular pressure development (dP/dt). For certain patients, further assistance of contractility can be achieved by variation of the inter-ventricular (“V-V”) interval. The V-V interval is the interval of time between LV and RV stimulation (or vice versa), which is a programmable parameter in currently available pulse generators (implantable, temporary and/or external). Optimization of the V-V interval can be performed on the guidance of echocardiographic or hemodynamic parameters as is known in the art.
In several studies it has been observed that LV pacing is hemodynamically superior or at least equal to bi-ventricular pacing. However, the inventors suggest that to date little or no attention has been paid to the mechanism(s) behind the observation.
In the above-referenced patent application to Hill, Hill appears to have discovered that in certain patients exhibiting symptoms resulting from congestive heart failure (CHF), cardiac output is enhanced by timing the delivery of an LV pacing pulse such that evoked depolarization of the LV is triggered by a sensed intrinsic depolarization of the RV. The conclusion was based on the notion that a “fusion” depolarization enhances cardiac output in cardiac patients where the RV depolarizes first due to intact A-V conduction of a preceding intrinsic or evoked atrial depolarization wave front, but the A-V conducted depolarization of the LV is unduly delayed. The fusion depolarization of the LV is attained by timing the delivery of an LV-PACE pulse to follow, in time, the intrinsic depolarization of the RV but to precede, in time, the intrinsic depolarization of the LV. Accordingly, an RV-PACE pulse is not delivered due to the inhibition of the RV-PACE upon the occurrence of a sensed RV-EVENT, allowing natural propagation of the wave front and depolarization of the septum, while an LV-PACE pulse is prematurely delivered in fusion with the RV depolarization.
However, due to a number of factors (e.g., the amount of time required for appropriate signal processing, confounding conduction delays or conduction blockage of a patient, electrode placement and the like) for a variety of patients A CRT delivery system that takes all these factors into consideration is needed.
Specifically, there is a need for structures, methods and processes to efficiently and chronically deliver and control of pacing therapy to effect ventricular fusion in cardiac patients who might otherwise not receive similar benefits from bi-ventricular CRT therapy.